Nystagmus

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Nystagmus
Dr. Huseynova Tukezban
Tukezban@gmail.com
Specialist in Strabismus and Refractive Cornea

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Historical Overview
“Nystazho” (Greek) – Wobbly head movements
of a sleepy or inebriated
individual.

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Definition
 Rhythm oscillations or tremors of eyes
 Occur independently of normal movements
 Usually of near equal amplitude in each phase
 May occur in one or both eyes

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Description
 Movement: Pendular (equal velocity in each direction) or Jerk
slow and fast component (recovery phenomenon aimed at
refixation)
*named according to fast phase
 Plane: Horizontal, vertical, torsional, or combination
 Amplitude: amount of excursion
 Frequency: cycles per time unit
 Manifestation: manifest, latent, manifest-latent

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Clinical Classification
“Nystagmus”
Physiological Pathological
Congenital Acquired
Optokinetic
Infantile Manifest
Vestibulor-Ocular Reflex
End gaze
Infantile
Manifest-latent
Infantile Latent
Functional
Visual loss
Neurological
Toxic

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Clinical Classification
Congenital Acquired
*Motor form
*Sensory form
*Latent form
*Manifest form
*Spasmus
Nutans
*Downbeat
*Upbeat
*See/Saw

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What Should we know?
 Refractive error correction
 Balance
 Vision often varies during the day
 Limitations
 Affected by emotional/physical factors such as stress, tiredness,
nervousness or unfamiliar surroundings.
 Poor depth perception, which can make it difficult to go up and down
stairs.

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Congenital Nystagmus

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Clinical Characteristics
Waveform
 Eye movement recordings demonstrate a slow drift
of the fovea away from the target (slow phase),
followed by a saccadic refixation (fast phase).

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Visual acuity
 In most patients with nystagmus, visual acuity is
decreased.
 Binocular acuity may be higher than monocular
 Visual acuity at near fixation often is dramatically better
than at distance fixation.
 The nystagmus may decrease or even disappear in
certain gaze positions
Visual deprivation amblyopia similar to bilateral
amblyopia caused by uncorrected high hypermetropia.

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Head position
A, Alternating head turn in a patient
with bidirectional null zone.
B, Improvement of visual acuity in
20°levoversion and dextroversion.

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Modulating Factor
 The amplitude of Nystagmus in many patients seems to diminish with
near fixation, attempted convergence, and increasing age.
 Convergence supresses the waveform in patients with congenital
nystagmus.
Vestibulo-Ocular Reflex Abnormalities
 The image of the optic nerve will not remain in the center of the viewing
field, allowing the VOR to be used to reduce the nystagmus intensity.
Oscillopsia
 Oscillopsia is an illusion that the visual enviroment is moving.

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Association with Strabismus
Nystagmus compensation (blockage)
syndrome
 Reduce the amplitude of nystagmus
 The sole purpose is improving visual acuity
 May produce anomalous head posture while
dampening the nystagmus
 Mostly seen in patients with early-onset
esotropia.
 These patients likely become esotropic
because of sustained convergence
 Pupillary constriction during esotropia will aid
the diagnosis

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 Occurs with uniocular fixation
 Upon occlusion, bilateral nystagmus with fast phase toward
uncovered eye
 Often noted in early childhood, usually in conjunction with
esotropia
 Acuity better using OU
 Using polarizing lens, +5.00 lens, etc. when assessing visual
acuity.
 Manifest Latent Nystagmus: present with both eyes open, but
actually only using one eye (suppression).
Latent and Manifest Nystagmus
Latent Nystagmus

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Latent Nystagmus
Manifest Nystagmus

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 The nystagmus has a reduced amplitude but remains when both eyes are
open.
 Common causes of manifest congenital nystagmus are:
Congenital Cataract
Congenital Glaucoma Aniridia
Achromatopsia
Down Syndrome
High Myopia

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 Most popular from pediatric neurophthalmic practise:
Optic nerve hypoplasia
Oculocutaneous albinism
Leber’s amaurosis

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Sensory Form
 Secondary to an afferent defect
 Inadequate image formation on macular due to
abnormal fixation
 Bilateral lens or cornea opacity, macular scars,
aniridia, achromatopsia.
 Onset: first weeks or months of life
 Severity of nystagmus tends to be proportional to visual
loss.

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Sensory Form
Clinical appearance
 Usually horisontal, sometimes vertical or rotary
 One side gaze may be more jerk
 2-4-6 “rule” of ocurence

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Sensory Form
2-4-6
“rule” ?
 Before 2 yrs – always nystagmus
 Before 4 yrs – maybe nystagmus
 After 6 yrs – never nystagmus

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Motor Form
Secondary to defect in efferent system
 Onset shortly after birth and persists for life
 No ocular anomalies
 Usually horisontal, sometimes vertical or torsional
Usually jerk
 Null point with improved vision in some
*Null point – the position of minimal movement may be straight ahead or may be
in an eccentric direction of gaze, either horizontally or vertically.

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Acquired Nystagmus

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Characteristics
Vertical
Intermittent
Disconjugate
Acquired
Globe Retraction
Associated with Vision Loss
Associated with other Neurological signs or symptoms

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Acquired childhood nystagmus
Spasmus Nutans
Clinical characteristics include the following three signs (onset 4-12 months);
The nystagmus is:
 Usually horizontal
 Can be vertical
 Can be rotary
 Can be mixed
 Usually rapid
 Usually low amplitude
 Can be bilateral but unequal
 Disappears in childhood
(usually before 3 years old)
Torticollis Head Nodding Nystagmus

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Opsoclonus
 Chaotic, bursts of multidirectional, high amplitude saccades. Appears like
flutter Neuroblastoma; also toxins, meningitis, increased ICP
Downbeat
 Downbeat nystagmus refers to the irregular downward jerking of the eyes
during downward gaze. It can signal lower medullary damage.

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Upbeat
 Convergence-retraction nystagmus refers
to the irregular jerking of the eyes back
into the orbit during upward gaze. It can
indicate midbrain tegmental damage.
See/Saw
 See/Saw nystagmus is the rapid, see-saw
Movement of the eyes: One eye appears
to rise while the other appears to fall. It
suggests an optic chiasm lesion

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Diagnosis
Clinical Examination Laboratory Evaluation
 Measurements of visual acuity
 Measurement of head turn
 Anterior segment evaluation
 Posterior segment evaluation
 Electroretinography
 Neuroimaging
 Eye movement recording
Grading System
 Grade 1 – present in right gaze only
 Grade 2 – present in right gaze and primary position
 Grade 3 – present in left gaze

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Treatment

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Non – Surgical treatment
 Amblyopia treatment
Penalisation with fogging
lens
Atropinisation
 Spectacle Correction
 Refractive error correction
 Minus lenses
 Partial field occlusion
 Prisms
 Head posture
 Visual acuity
Fresnel Prism
20△

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Non – Surgical treatment
 Pharmocologic Treatment
 IV muscarinic antagonist
 Clonazepam
 Baclofen
 Ethanol
 Diethylproprianate
 Dexedrine
Side effects
limit usefulness

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Surgical treatment
 Goals of surgical treatment
 Improve vision function
 Improve secondary anomalous head position (AHP)
 Improve appearance
 Decrease or Eliminate Oscillopsia

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Surgical treatment
I. Surgery WITH AHP
Horizontal AHP
Right or Left Face Turn
i.e. Left head turn, Dextroversion
Recess = RLR, LMR
Resect = RMR, LLR
Procedure
* Recess muscles that
function in a direction
opposite the face turn
* Resect muscles that
function in the same
direction as the face
turn

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Surgical treatment
 Kestenbaum-Anderson techniques
 For horizontal anomalou head posture
Kestenbaum – resect yoked muscles
Anderson – recess yoked rectus muscles

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Surgical treatment

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Surgical treatment
30º Turn = 40% 45º Turn = 60%
Recess MR
Resect MR
Recess LR
Resect LR
5
6
7
8
K-A
7
8.4
9.8
11.2
40% 60%
8
9.6
11.2
12.8

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Surgical treatment
I. Surgery WITH AHP
Vertical AHP
Chin up or Chin down
i.e. Chin up = Recess IR,
Resect SR
Chin down = Resect IR,
Recess SR
Procedure
* Shift eyes toward
chin deviation

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Surgical treatment
I. Surgery WITH AHP
Head tilt
i.e. Right Tilt
transpose nasal: RSR, LIR
transpose temporal: LSR, RIR
Procedure
* Transpose vertical rectus muscles opposite to head tilt
Right or Left Head Tilt
 AHP with Strabismus
 Surgery to align eyes and correct AHP

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Surgical treatment
II. Surgery for NO AHP
NO AHP with Near fixation damping
Artificial Divergence
(promotes convergence damping)
Procedure
* Recess MR both eyes 3.0-4.0mm (+/- posterior
fixation suture)
* Trial of base out prism with myopic correction
(for convergence induced accomodation) may be
helpful.

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Surgical treatment
II. Surgery for NO AHP
NO AHP and NO Near fixation damping
 4 muscles Tenotomy
Detach and then reattach 4 horizontal
rectus muscles at original
 Large 4 muscles Recession
Recess MR 8-10 mm OU;
Recess LR 10-12 mm OU

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Surgical treatment
III. Miscellaneous procedures
Retrobulbar Botulinum Toxin
 For acquired, intractable oscillopsia and failed
medical treatment
 For bilateral oscillopsia (patch affected eye if
unilateral
 Repeat injections needed, typically every 3-12
months
Superior Oblique Myokymia Surgery
Procedure
* Ipsilateral Superior Oblique Tenotomy
and Inferior Oblique Myectomy
* Note: Procedure may induce secondary
vertical deviation.

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Surgical treatment
Summary
Individualize to Each patient
Understand patient expectations
Treatment modalities evolving
Much to learn about treatment of
nystagmus

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Thank You

Nystagmus

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